Cholesterol has a reputation problem. We tend to think of it as the enemy, but your body makes it for a reason. Every cell membrane relies on it, and it’s the building block for key hormones like oestrogen, progesterone, and corticosteroids. You also get cholesterol from your diet. The real issue isn’t cholesterol itself — it’s where it ends up. 

In the early 1900s, pathologists examining people who died from heart attacks found arteries lined with cholesterol-rich plaques, complete with visible crystals. By the 1950s and 60s, research confirmed that high cholesterol in the blood is a major risk factor for heart disease. When plaques build up, they trigger inflammation and clotting, potentially cutting off blood supply to the heart. 

Cholesterol doesn’t travel freely in the bloodstream — it’s packaged into tiny particles called lipoproteins. These act like delivery vehicles, carrying cholesterol around the body. Drugs such as statins reduce cholesterol production and improve its clearance, saving millions of lives. Exercise, diet, and blood pressure control are also critical, especially since high blood pressure and high cholesterol together significantly increase risk. 

But there’s more to the story. Around one in 250 people have inherited conditions that leave them with very high cholesterol levels. And as listener Tara asked in her email to the podcast, what about Lipoprotein little a — or Lp(a)? 

Lp(a) is a specialised lipoprotein that can increase inflammation and clot formation. Elevated levels are linked to a greater risk of heart attack — even if your standard cholesterol numbers look normal. That means measuring total cholesterol alone may not tell the full story. 

On this week’s podcast Professor Luke O’Neill explores why cholesterol is essential, how it becomes dangerous, and why particles like Lp(a) could be key to identifying hidden heart risk. 

Have a science question you’d like answered? Email [email protected] and it might feature in a future episode.